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Laboratory Tests to Determine the Cause of Hypokalemia and Paralysis

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Laboratory Tests to Determine the Cause of Hypokalemia and Paralysis ORIGINAL INVESTIGATION Laboratory Tests to Determine the Cause of Hypokalemia and Paralysis Shih-Hua Lin, MD; Yuh-Feng Lin, MD; Dung-Tsa Chen, PhD; Pauling Chu, MD, PhD; Chin-Wang Hsu, MD; Mitchell L. Halperin, MD Background: Hypokalemia and paralysis may be due tients in the non-HPP group had urine potassium con- to a short-term shift of potassium into cells in hypoka- centration values less than 20 mmol/L. Although the po- lemic periodic paralysis (HPP) or due to a large deficit tassium concentration was significantly lower in the HPP of potassium in non-HPP. Failure to make a distinction group, there was some overlap. In contrast, the transtu- between HPP and non-HPP may lead to improper man- bular potassium concentration gradient and potassium- agement. Therefore, we evaluated the diagnostic value creatinine ratio differentiated patients with HPP vs non- of spot urine tests in patients with hypokalemia and pa- HPP. Although only a mean±SD of 63±36 mmol of ralysis during 3 years. potassium chloride was administered in the patients with HPP, rebound hyperkalemia (Ͼ5 mmol/L) occurred in Methods: Before therapy, the urine potassium concen- 19 (63%) of these 30 patients. tration, potassium-creatinine ratio, and transtubular po- tassium concentration gradient were determined in a sec- Conclusions: Calculating the transtubular potassium ond voided urine sample. concentration gradient and potassium-creatinine ratio pro- vided a simple and reliable test to distinguish HPP from Results: Forty-three patients with hypokalemia and pa- non-HPP. Minimal potassium chloride supplementa- ralysis were identified: 30 had HPP and 13 had non- tion should be given to avoid rebound hyperkalemia in HPP. There was no significant difference in the plasma patients with HPP. potassium or bicarbonate concentrations and in the pH of arterial blood between the 2 groups. All but 2 pa- Arch Intern Med. 2004;164:1561-1566 YPOKALEMIA AND PARALY- been misdiagnosed as having HPP.9 Be- sis (HP) is a potentially cause hypokalemia is the primary bio- reversible medical emer- chemical abnormality in patients with HP, gency.1 Morbidity and measurements of the urinary excretion of mortality are related to potassium were the focus of our evalua- Hcomplications secondary to hypokalemia tion. To establish whether renal potas- such as a cardiac arrhythmia or respira- sium wasting is present in these medical tory failure.2 Although there are many po- emergencies, one cannot wait for a pro- tential causes of hypokalemia, there are far longed, timed urine collection. Hence, a From the Division of fewer entities in the differential diagno- second voided spot urine collection be- Nephrology, Department of sis of HP (Table 1).1 Hypokalemia and fore initiation of therapy is the optimum Medicine (Drs S. H. Lin, Y. F. Lin, and Chu), and paralysis can be divided into 2 types, hy- sample to examine. In this study, we Department of Emergency pokalemic periodic paralysis (HPP) due to sought to evaluate the diagnostic value of 3-5 Medicine (Dr Chen), a short-term shift of potassium into cells spot urine tests in patients with HP. Tri-Service General Hospital, and non-HPP resulting from a large defi- National Defense Medical cit of potassium.6,7 Center, Taipei, Taiwan; The differential diagnosis in a pa- METHODS Biostatistics Unit, UAB tient with HP can be challenging, but it is Comprehensive Cancer Center, important to make the diagnosis promptly STUDY SUBJECTS University of Alabama, because different therapies are required for Birmingham (Dr Hsu); and each type. Although some features dis- The study protocol was approved by the Eth- Renal Division, St Michael’s ics Committee on Human Studies at Tri- Hospital, University of Toronto, cerned on patient history such as a posi- Service General Hospital, Taiwan. Taipei, In- Toronto, Ontario tive family history or a recurrent episode formed consent was obtained from each patient. (Dr Halperin). The authors can be helpful, the clinical features of HPP Forty-three new patients with HP were en- have no relevant financial and non-HPP are almost indistinguish- rolled in this study between January 1, 2000, interest in this article. able.8 Many patients with non-HPP have and December 31, 2002. Hypokalemia and pa- (REPRINTED) ARCH INTERN MED/ VOL 164, JULY 26, 2004 WWW.ARCHINTERNMED.COM 1561 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 Table 1. Patient Characteristics and Final Diagnosis No. of Age, Patient Group Patients Mean ± SD, y Male-Female Hypokalemic periodic paralysis (n = 30) Thyrotoxic periodic paralysis 20 28 ± 8 20:0 Sporadic periodic paralysis 9 28 ± 7 8:1 Familial periodic paralysis 1 19 1:0 Non–hypokalemic periodic paralysis (n = 13) Primary aldosteronism 1 34 1:0 Gitelman syndrome 4 24 ± 2 3:1 Licorice ingestion 1 72 1:0 Distal renal tubular acidosis 5 38 ± 23 2:3 Fanconi syndrome with proximal renal tubular acidosis 1 42 1:0 Profound diarrhea 1 47 1:0 ralysis was defined as an acute loss of muscle power with an ANALYTICAL TECHNIQUES inability to ambulate and a plasma potassium concentration that was less than 3 mmol/L on presentation. The paralysis tended Arterial blood gases were measured by an ABL 510 (Radiometer, to involve the muscles of the extremities and limb girdles. Copenhagen, Denmark). Biochemical values, including serum and urine creatinine, urea nitrogen, albumin, total calcium, inor- DEFINITIONS ganic phosphate, magnesium, sodium, potassium, and chloride, were determined by automated methods (AU 5000 chemistry ana- Hypokalemic Periodic Paralysis lyzer; Olympus, Tokyo, Japan). Plasma osmolality (Posm) and urine osmolality (Uosm) were measured by freezing-point depression (Ad- Hypokalemic periodic paralysis must be defined on clinical grounds. vanced Instruments Inc, Needham Heights, Mass). There were 4 elements to the diagnosis. First, a positive family history, recurrent clinical pattern, or evidence of hyperthyroid- CALCULATIONS ism made HPP a likely diagnosis. The absence of the intake of agents that could cause a shift of potassium into cells was also The transtubular potassium concentration gradient (TTKG) was important in this context. Second, if there was no indication of calculated as previously described ([urine/plasma 10 other diseases known to be associated with potassium wasting, potassium]/[urine/Posm]). It is not physiologically valid to cal- 11 again HPP would be suspected. Third, if the patients required less culate the TTKG if the Uosm is less than the Posm. The urine than 1.5 mmol of potassium chloride per kilogram of body weight potassium-creatinine ratio, an index of the potassium excre- to return their plasma potassium concentration to the normal tion rate, was calculated using their respective concentrations range, this supported the diagnosis of HPP. Fourth, the absence in millimoles per liter. of an acid-base disorder strengthened the diagnosis of HPP.9 STATISTICAL ANALYSIS Non–Hypokalemic Periodic Paralysis The mean±SD was calculated for patient characteristics and Non–hypokalemic periodic paralysis was suspected if none of the diagnostic measures. A 2-sample t test was used to compare 4 findings in the previous paragraph were present, if there was the differences in diagnostic measures, recovery times, and an explanation for a large deficit of potassium, if more than 3 amount of potassium chloride that was administered in mmol/kg of potassium was needed to correct the plasma po- the HPP and non-HPP groups. Scatterplots were used for tassium concentration to the normal range, and if an acid-base data visualization to explore the cutoff values for diagnostic disorder was present.9 measures. PROCEDURES RESULTS A spot urine sample was collected before therapy by self- voiding if possible or with a Foley catheter if the patient was Forty-three patients with a severe degree of hypokale- unable to urinate. To avoid the possibility of obtaining urine mia (range, 1.5-2.6 mmol/L) and paralysis were in- that represented a mixture of urine from before the onset of cluded in the study. The male-female ratio was 38:5; their the attack and at the time of the attack, urine in the bladder on ages ranged from 18 to 78 years. Of the 43 patients, 30 presentation was discarded and a second voided urine speci- were in the HPP group and 13 in the non-HPP group. men was collected during the next hour. An arterial blood sample The mean age (28±8 vs 37±18 years) and body mass in- was collected in all the patients; venous blood samples were dex (calculated as weight in kilograms divided by the collected through an indwelling catheter. All of the patients re- square of height in meters) (22.0±2.3 vs 21.5±2.1) were ceived intravenous potassium chloride administration at a rate not significantly different between the 2 groups. In the of 10 mmol/h until muscle strength had recovered and the pa- HPP group, 20 patients had thyrotoxic periodic paraly- tient could ambulate. The plasma potassium concentration was sis (TPP) (Table 1). Three known dihydropyridine- measured hourly during the attack and for 6 hours after recov- ␣ ery. The recovery time was defined as the time required from sensitive calcium channel 1 subunit (CACNA1S) gene the initiation of potassium chloride therapy to the recovery of mutations (R528H, R1239H, and R1239G) were ana- sufficient muscle strength to ambulate. The quantity of potas- lyzed in the patients with TPP, sporadic periodic paraly- sium chloride administered was recorded. sis (SPP), and familial periodic paralysis (FPP).
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